A technique necessary for apolipoprotein metabolic studies is to quantitate apolipoproteins. We developed an ELISA essay for apoB and are presently developing ones for apoA-I, A-II, C-II, and E. ApoE binds to the LDL receptor in vitro. In vivo studies of apoE were performed in subjects who lack the LDL receptor. The fractional catabolic rate (FCR) of apoE was normal indicating the LDL receptor is unlikely to be an important site of catabolism for apoE. Two forms of apoE, apoE2 and apoE2*, associated with type III hyperlipoproteinemia (HLP) were evaluated by in vivo kinetic studies. The metabolism of apoE2 and apoE2* were the same and the FCR for both significantly slower than for normal apoE. The metabolism of apoA-I has been investigated in a number of subjects. In type V HLP subjects, who have decreased apoA-I levels, the FCR of apoA-I was increased with a normal synthesis rate. Tangier disease subjects have decreased levels of apoA-I with a relative increase of proapoA-I. The rate of conversion of proapoA-I to mature apoA-I was normal and the relative increase in proapoA-I was due to rapid catabolism of mature apoA-I. A genetic variant of apoA-I with one additional unit of negative charge was investigated and found to have a normal FCR. There are two forms of apoB in plasma, apoB-48 of intestinal origin and apoB-100 of hepatic origin. Their metabolism was investigated in subjects lacking the LDL receptor. VLDL apoB-48 was catabolized at a normal rate with little conversion to IDL and LDL, similar to normal subjects. VLDL apoB-100 had a slower FCR with increased conversion to IDL and LDL compared to normals. Therefore, the LDL receptor does not have a role in apoB-48 metabolism but does regulate apoB-100 metabolism. Subjects homozygous for apoE2 have decreased LDL and apoB concentrations. LDL apoB from these subjects was catabolized at a decreased FCR compared to normal LDL apoB. Also, these subjects catabolized both normal and their own LDL apoB more rapidly than normals. The decreased LDL apoB levels were due to both a decreased production rate and an increased FCR. Therefore, apoE has complex effects on LDL apoB metabolism.